DIM attenuates TGF-β1-induced myofibroblast differentiation in neonatal rat cardiac fibroblasts.

3,3'-Diindolylmethane (DIM) reduced the differentiation of cardiac fibroblasts into myofibroblasts by inhibiting key signaling pathways.

• DIM blunted the conversion of cardiac fibroblasts into myofibroblasts induced by transforming growth factor β1 (TGF-β1).
• The treatment decreased both mRNA and protein levels of α-smooth muscle actin (α-SMA).
• DIM significantly lowered the mRNA expression of fibrosis markers, including Collagen I, Collagen III, and connective tissue growth factor (CTGF).
• DIM attenuated the phosphorylation of AKT and glycogen synthase kinase-3β (GSK-3β), which are activated by TGF-β1.
• Findings suggest that DIM may be a potential agent to mitigate myofibroblast differentiation and excessive extracellular matrix production.

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